In details, we have recently demonstrated that the HDACi vorinostat, in combination with the EGFR-tyrosine kinase inhibitor gefitinib, induced synergistic inhibition of proliferation, migration and invasion as well as induction of apoptosis, in preclinical models of SCCHN, including cancer cell lines resistant to gefitinib and characterized by mesenchymal markers and phenotype. This evidence concerns the gene EGFR and head and neck squamous cell carcinoma.